2014
DOI: 10.1016/j.expneurol.2014.02.024
|View full text |Cite
|
Sign up to set email alerts
|

Repurposing Reelin: The new role of radial glia, Reelin and Notch in motor neuron migration

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3

Citation Types

0
3
0

Year Published

2019
2019
2023
2023

Publication Types

Select...
3
1

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(3 citation statements)
references
References 79 publications
0
3
0
Order By: Relevance
“…The aforementioned techniques have allowed us to establish that neuroblasts, originating from the neuroepithelium, subsequently migrate in a targeted manner through amoeboid movements in various directions towards their sites of further differentiation along the radial glial fibers [5]. There is a viewpoint that these "guiding" glial cells disappear after the maturation of neurons.…”
Section: Introductionmentioning
confidence: 99%
“…The aforementioned techniques have allowed us to establish that neuroblasts, originating from the neuroepithelium, subsequently migrate in a targeted manner through amoeboid movements in various directions towards their sites of further differentiation along the radial glial fibers [5]. There is a viewpoint that these "guiding" glial cells disappear after the maturation of neurons.…”
Section: Introductionmentioning
confidence: 99%
“…The mechanism underlying this unusual combination of both central and peripheral motor impairment is unknown, but it most probably involves a common genetic insult affecting basic cellular processes regulating the development of MNs and cortical projection neurons (PNs). During the embryonic period, PNs and MNs are generated in germinal ventricular zones then migrate radially to reach their final anatomical position and interestingly, they share common molecular regulators [5][6][7] . Here, we identify a missense mutation in the MCF.2 Cell Line Derived Transforming Sequence (MCF2) gene in a boy with CBPS associated to lower MN dysfunction.…”
Section: Introductionmentioning
confidence: 99%
“…In the reeler phenotype mice, the Reln gene is missing 6 and therefore the process of neuron migration and brain architecture are compromised. This knockout results in an inverted cerebral cortex 7 . The Reln gene, located on chromosome 7 in humans, encodes reelin (RELN) - a large (385 kDa) signal glycoprotein localized in the extracellular matrix.…”
Section: Introductionmentioning
confidence: 99%